Deregulation of the nutrient sensitive mTOR signaling pathway has been recently involved in several age-related diseases, and pharmacological blockade of mTOR extends longevity in model organisms and in mice. Mechanistic studies in vitro have shed light on the role of mTOR-dependent growth signals in promoting senescence and exhaustion of quiescent stem cells, thus linking excess nutrients to tissue ageing. Novel findings add complexity to this theoretical framework, revealing that mTOR cooperates with autophagy to promote the "secretory phenotype" of senescent cells and the release of factors known to contribute to defective renewal and dysfunction of aging tissues. Thus, both cell autonomous and cell non-autonomous mechanisms link unchecked mTOR activity to cell senescence and by extension to the aging process.